Abcam, ab259062, Human PRKAR1B knockout HeLa cell lysate

Size: 1Kit
PRKAR1B KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon2.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon2.,
Disease:Adenocarcinoma

Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-PRKAR1B, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
PRKAR1B also known as the regulatory subunit type I beta of protein kinase A (PKA) plays an important role in the regulation of cAMP-dependent PKA activity. This protein has a molecular mass of approximately 44 kDa. It binds to the catalytic subunit of PKA inhibiting its activity until cAMP binds which then triggers a conformational change and release of the active catalytic subunit. PRKAR1B is expressed in various tissues with notable abundance in the brain highlighting its significance in neuronal signaling.
Biological function summary
PRKAR1B functions as part of the PKA holoenzyme complex which includes both regulatory and catalytic subunits. The regulatory subunit PRKAR1B directly controls when and where PKA catalytic activity occurs influencing multiple cellular responses. This protein modulates processes like glycogen lipid and protein metabolism by contributing to the precise regulation of cAMP signaling pathways. Its activity affects a range of fundamental cellular functions indicative of its presence in diverse tissues.
Pathways
PRKAR1B is intricately involved in the cAMP signaling pathway and the MAPK/ERK pathway. The cAMP pathway is important for transferring the signals of many hormones and neurotransmitters where PRKAR1B regulates transient PKA activation. In the MAPK/ERK pathway PRKAR1B indirectly influences cellular growth and differentiation by modulating secondary messengers. Proteins such as the catalytic subunits of PKA and CREB a transcription factor interact with PRKAR1B illustrating its central role in cellular responses to external signals.
PRKAR1B has been associated with neurodegenerative diseases like Alzheimer’s and mood disorders such as major depressive disorder. Altered regulation of the cAMP signaling pathway influenced by PRKAR1B affects neuronal survival and function potentially leading to neurodegeneration. Additionally imbalances in PRKAR1B-mediated pathways can contribute to mood disorders. Proteins such as the catalytic subunits of PKA and BDNF (brain-derived neurotrophic factor) interact with PRKAR1B in these contexts indicating its potential as a therapeutic target.